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Acid-base Balance (ABB)

Acid-base Balance (ABB). Vladimíra Kvasnicová. Definition - REPETITION. pH acid base dissociation constant buffers. The figure was found at http://www.colorado.edu/kines/Class/IPHY3430-200/14fluid.html (April 2007). the border between strong and weak acid K = 10 -2.

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Acid-base Balance (ABB)

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  1. Acid-base Balance(ABB) Vladimíra Kvasnicová

  2. Definition - REPETITION • pH • acid • base • dissociation constant • buffers

  3. The figure was found at http://www.colorado.edu/kines/Class/IPHY3430-200/14fluid.html (April 2007)

  4. the border betweenstrong and weak acid K = 10-2 = nedisociovaná kyselina = volný H+ = volný anion The figure was found at http://www.colorado.edu/kines/Class/IPHY3430-200/14fluid.html (April 2007)

  5. + 3 HCl The figure was found at http://www.colorado.edu/kines/Class/IPHY3430-200/14fluid.html (April 2007)

  6. [CO2] =  x pCO2  = 0,226 for pCO2 expressed in kPa  = 0,03 for pCO2 expressed in mmHg

  7. Dissociation constant and buffer pH ! the best buffering properties: pH = pK ± 1 ! • pH = pK + log (1 / 1)  pH = pK • pH = pK + log (10 / 1)  pH = pK + 1 • pH = pK + log (1 / 10)  pH = pK - 1

  8. Calculate the ratio of components of the phosphate buffer (HPO42- / H2PO4-)pK2 = 7,0 if a) pH = 7,4 (blood) b) pH = 7,0 (cell) c) pH = 6,0 (urine)

  9. The source and fate of acids / bases • source of acids: metabolism • source of bases: food • fate: • transformation by the metabolism • excretion

  10. ~ 20 000 mmol / den The figure has been adopted from J.Koolman, K.H.Röhm / Color Atlas of Biochemistry, 2nd edition, Thieme 2005

  11. The metabolism produces acids: carbon skeleton→ CO2+H2O → HCO3-+ H+ • saccharides→ glucose → pyruvate, lactate + H+ • triacylglycerols→ fatty acids, ketone bodies + H+ • phospholipids→ phosphate + H+ • proteins→ amino acids → sulfate, urea + H+

  12. Acids formed in the human body • metabolic (nonvolatile) acids → excretion by the kidneys • glucose →lactic acid lactate + H+ • fatty acids → ketone bodies: acetoacetic acid acetoacetate + H+ -hydroxybutyric acid  -hydroxybutyrate + H+ • amino acids Cys and Met →H2SO4→ sulfate + 2H+ • phospholipids →H3PO4 HPO42- + 2H+ • respiratory (volatile) acid → excretion by the lungs • CO2 + H2O  H2CO3HCO3- + H+

  13. The order of systems whichparticipate in ABB • buffers(changes of pH caused by common metabolism) • the lungs (CO2) • the kidneys (H+, HCO3-) • blood pH can be also affected bythe liver (synthesis of urea, metabolism of lactate) and the heart(oxidation of ketone bodies and lactate)

  14. The liver – detoxication of ammonia according to the ABB state amino acids LIVER, MUSCLE carbon skeleton LIVER urine urine favourized during alkalemia favourized during acidemia The figure has been adopted from: Klinická biochemie. Požadování a hodnocení biochemických vyšetření. Karolinum, Praha, 1998. ISBN 80‑7184‑649‑3

  15. GLUTAMINE cycle in the liver The figure has been adopted from Devlin, T. M. (editor): Textbook of Biochemistry with Clinical Correlations, 4th ed. Wiley‑Liss, Inc., New York, 1997. ISBN 0‑471‑15451‑2

  16. Principal buffer systems

  17. Blood buffers - overview • bicarbonate buffer: HCO3-/CO2 pK(H2CO3) = 6,1 24 mM • phosphate buffer: HPO42-/H2PO4- pK(H2PO4-) ≈ 7,0 1 mM • hemoglobin: Hb-/Hb-H+ pK(HHbO2) = 6,17 pK(HHb) = 7,82 160g/L • proteins: protein/protein-H+ 70g/L pK = 4 – 12(mainly Asp, Glu and His)

  18. Blood buffers

  19. O2 Excretion of CO2 by the lungs O2 http://science.kennesaw.edu/~jdirnber/Bio2108/Lecture/LecPhysio/42-29-BloodCO2Transport-AL.gif (March 07)

  20. Excretion of H+ by the kidneys (I) http://www.colorado.edu/kines/Class/IPHY3430-200/14fluid.html (April 2007)

  21. Excretion of H+ by the kidneys (II) http://www.colorado.edu/kines/Class/IPHY3430-200/14fluid.html (April 2007)

  22. Excretion of H+ by the kidneys (III) http://www.colorado.edu/kines/Class/IPHY3430-200/14fluid.html (April 2007)

  23. Urine buffers • 1 excreted H+ 1 reabsorbed HCO3- • NH3 + H+→ NH4+(50 mmol H+/day) • H+ + HPO42-→ H2PO4-(20 mmol H+/day)

  24. ABB disorders The figure has been adopted from J.Koolman, K.H.Röhm / Color Atlas of Biochemistry, 2nd edition, Thieme 2005

  25. CO2 produced by metabolic reactions HCO3- regenerated in the kidneys HCO3- lost by buffering endogenously produced acids CO2 excreted by the lungs http://romerosnap1.phol.cwru.edu/AcidBase-SOMy1.htm (April 2007)

  26. Primary disorders of ABB Resp. Mtb. pCO2 HCO3- http://romerosnap1.phol.cwru.edu/AcidBase-SOMy1.htm (April 2007)

  27. 24 mM http://romerosnap1.phol.cwru.edu/AcidBase-SOMy1.htm (April 2007)

  28. Compensation = effort to readjust plasma pH back toward normal • one system compensates disfunction of the other system • respiratory disorders are compensatedby the kidneys(3-5 days) • metabolic disorders are compensatedby the lungs(12-24 hours) or corrected by the kidneys

  29. EXAMPLE OF COMPENSATION: metabolic alkalosis uncompensated compensated http://romerosnap1.phol.cwru.edu/AcidBase-SOMy1.htm (April 2007)

  30. Physiological values of ABB(Astrup) pH 7,36 - 7,44 pO2 8,9 - 14,7 kPa pCO2 4,80 - 5,90 kPa HCO3- 24 ± 2 mM BE 0 ± 2,5 mM

  31. Respiratory Acidosis (RAc) cause:hypoventilation  CO2 + H2O  H2CO3 HCO3- + H+ buffering: H+ + Hb  Hb-H+ loss of base result: * increase of pCO2 decrease of pH * increase of HCO3- and decrease of other buffer bases, especially of Hb BE = 0 when pO2 lactate  (+ MAc) compenstaion:  resorption of HCO3- in the kidneys acidic urine positive BE

  32. Respiratory Alkalosis (RAl) cause:hyperventilation   CO2+ H2O  H2CO3 HCO3- + H+ buffering: Hb-H+  Hb + H+  increase of bases reult: * decrease of pCO2  increase of pH * decrease of HCO3- and increase of other buffer bases  BE = 0 compensation: increased excretion of HCO3- by the kidneys  negative BE

  33. Respiratory disorders deviation from equilibrium to other isobars A (C) = primary imbalance B (D) = compensated The figure has been adopted from: Devlin, T. M. (editor): Textbook of Biochemistry with Clinical Correlations, 4th ed. Wiley‑Liss, Inc., New York, 1997. ISBN 0‑471‑15451‑2

  34. Metabolic Acidosis (MAc) causes: 1) overproduction of acids (H+) in mtb    increased anion gap 2) increased excretion of HCO3-  normal anion gap ad1) metabolism produces excess of acids   H+ buffering: H+ + HCO3-  H2CO3  H2O + CO2  excretion of CO2: hyperventiltion (= compensation) H+ are also buffered by bases of nonbicarbonate buffers  decrease of BE (HCO3- and other buffer bases) ad2) loss of HCO3- e.g. diarrhoea, inhibitors of CA

  35. Metabolic Acidosis (II) result: * decrease of pH * negative BE * acidic urine ( phosphates and NH4+),  decreased excretion HCO3- * deep breathing (stimulation of the respiratory centre by high concentration ofH+)  later:  pCO2 (= compensation) compensation: hyperventilation  other decrease of HCO3-

  36. Metabolic Alkalosis (MAl) cause:1)increased excretion of protons (e.g. vomitting,  resorption of NaHCO3) 2)increased ingestion of bases buffering:  H+  CO2 + H2O  H2CO3  HCO3- + H+ other buffers  H+   HCO3- and other buffer bases  positive BE result: * increase of pH * positive BE *  K+ in blood  heart beat imbalance compensation: hypoventilation

  37. Metabolic disorders deviation from equilibrium proceeds at the same isobar E (G) = primary imbalance F (H) = compensated The figure has been adopted from:Devlin, T. M. (editor): Textbook of Biochemistry with Clinical Correlations, 4th ed. Wiley‑Liss, Inc., New York, 1997. ISBN 0‑471‑15451‑2

  38. Kalemia(= concentration of K+ in blood) 3,8-5,3 mM • acidosis release of K+ from cells  hyperkalemia  loss of K+ with urine (quick alkalization of the organism by treatment can cause consequent hypokalemia  danger of heart beat imbalance) • alkalosis K+ replaces H+ in cells  decrease of K+ in blood hypokalemia; K+ is excreated into urine instead of H+ (exchange with Na+)

  39. Case 1 A 70 year old man suffering from chronic lung disease, was admitted with an acute exacerbation. After admission testing (A), vigorous physiotherapy and medical treament were instituted, but his condition deteriorated (B). Artificial ventilation was started.6 hours later results were (C).After 12 hours he had a seizure (D).   A B C D pH 7,30 7,24 7,40 7,54 pCO2(kPa) 9,47 10,93 7,73 5,73 HCO3-(mM) 35 35 34 35

  40. Case 2 A young woman was admitted unconscious, following a head injury. X-Ray showed a skull fracture and CT showed extensive cerebral contusions. There was no change over three days. A B pH 7,52 7,48 pCO2(kPa) 3,47 3,87 HCO3-(mM) 22 19

  41. Case 3 A patient with vague symptoms, fever and hyperventilation presented in the Emergency Room: Na+ 140 mM K+ 3,5 mM Cl- 102 mM HCO3- 13 mM pH 7,39 pCO2 2,67 kPa

  42. Case 4 A 45 year old man was admitted with a history of persistent vomiting. He had a long history of dyspepsia which had gone untreated except with proprietary remedies. Examination revealed dehydration and shallow respirations.   pH 7,56 pCO2(kPa) 7,20 HCO3-(mM) 45 K+(mM) 2,8

  43. Case 5 A 23 year old mechanic was brought to ER 12 hours after drinking antifreeze. He was agitated and confused. His sclerae were icteric. Na+(mM) 137 K+(mM) 5,4 Cl-(mM) 95 HCO3-(mM) 4 glukóza (mM) 2,5 pH 6,95 pCO2(kPa) 2,0

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